Autophagy is a conserved catabolic process that degrades cytoplasmic constituents and organelles in the lysosome. It is a key mechanism for protein homeostasis and quality control, and plays a crucial role in both nutrient-replete and starvation conditions by mobilizing diverse cellular energy and nutrient stores such as lipids, carbohydrates, and iron. Processes like lipophagy, glycophagy, and ferritinophagy enable cells to salvage key metabolites to sustain core anabolic functions. Autophagy is also involved in the degradation of damaged and dysfunctional proteins and organelles, and is essential for maintaining cell homeostasis. It works in conjunction with the ubiquitin–proteasome system (UPS) to regulate protein quality control. Autophagy is also important for the degradation of misfolded or damaged proteins in the endoplasmic reticulum (ER), and for the clearance of aggregated proteins in postmitotic tissues such as nerve and muscle. Autophagy has a pro-survival role during ER stress as it acts as an alternative mechanism for the clearance of misfolded or damaged proteins that cannot be cleared by the unfolded protein response. Autophagy is also involved in the degradation of other organelles such as ribosomes, nuclei, and ER, and in the selective degradation of intracellular pathogens (xenophagy) and transient macromolecular structures within cells. Autophagy is important for energy metabolism, as it can mobilize diverse cellular energy stores such as carbohydrates, lipids, and ferritin to replenish metabolites during both normal and stressed conditions. Autophagy-derived amino acids are important for enabling protein synthesis in mammalian cells, and are also used for the synthesis of total proteins and specific proteins, including Arg1p and Hsp26p, which mitigate nitrogen depletion. Autophagy also supports mitochondrial function in yeast cells by upregulating proteins involved in respiration and reactive oxygen species scavenging. Autophagy is also involved in the degradation of lipids, which is important for energy production and biosynthesis. Autophagy is important for the degradation of glycogen, which represents the major form of stored glucose in the liver. Autophagic degradation of glycogen is a crucial mechanism to maintain glucose homeostasis in response to increased demand for this carbohydrate. Autophagy is also involved in the regulation of energy homeostasis in various tissues, including adipose tissue, skeletal muscle, and the liver. Autophagy has been shown to play a role in the differentiation of white and brown adipocytes, and in the regulation of energy balance. Autophagy is also involved in the regulation of glucose metabolism in the hypothalamus, where it controls food intake and energy balance by regulating hypothalamic lipid metabolism. Autophagy is also involved in the regulation of energy homeostasis in the pro-opiomelanocortin (POMC)Autophagy is a conserved catabolic process that degrades cytoplasmic constituents and organelles in the lysosome. It is a key mechanism for protein homeostasis and quality control, and plays a crucial role in both nutrient-replete and starvation conditions by mobilizing diverse cellular energy and nutrient stores such as lipids, carbohydrates, and iron. Processes like lipophagy, glycophagy, and ferritinophagy enable cells to salvage key metabolites to sustain core anabolic functions. Autophagy is also involved in the degradation of damaged and dysfunctional proteins and organelles, and is essential for maintaining cell homeostasis. It works in conjunction with the ubiquitin–proteasome system (UPS) to regulate protein quality control. Autophagy is also important for the degradation of misfolded or damaged proteins in the endoplasmic reticulum (ER), and for the clearance of aggregated proteins in postmitotic tissues such as nerve and muscle. Autophagy has a pro-survival role during ER stress as it acts as an alternative mechanism for the clearance of misfolded or damaged proteins that cannot be cleared by the unfolded protein response. Autophagy is also involved in the degradation of other organelles such as ribosomes, nuclei, and ER, and in the selective degradation of intracellular pathogens (xenophagy) and transient macromolecular structures within cells. Autophagy is important for energy metabolism, as it can mobilize diverse cellular energy stores such as carbohydrates, lipids, and ferritin to replenish metabolites during both normal and stressed conditions. Autophagy-derived amino acids are important for enabling protein synthesis in mammalian cells, and are also used for the synthesis of total proteins and specific proteins, including Arg1p and Hsp26p, which mitigate nitrogen depletion. Autophagy also supports mitochondrial function in yeast cells by upregulating proteins involved in respiration and reactive oxygen species scavenging. Autophagy is also involved in the degradation of lipids, which is important for energy production and biosynthesis. Autophagy is important for the degradation of glycogen, which represents the major form of stored glucose in the liver. Autophagic degradation of glycogen is a crucial mechanism to maintain glucose homeostasis in response to increased demand for this carbohydrate. Autophagy is also involved in the regulation of energy homeostasis in various tissues, including adipose tissue, skeletal muscle, and the liver. Autophagy has been shown to play a role in the differentiation of white and brown adipocytes, and in the regulation of energy balance. Autophagy is also involved in the regulation of glucose metabolism in the hypothalamus, where it controls food intake and energy balance by regulating hypothalamic lipid metabolism. Autophagy is also involved in the regulation of energy homeostasis in the pro-opiomelanocortin (POMC)